As shown in Figure 3I, FAS, CASP9, and BBC3 were significantly upregulated in Eto treated GBM cells with Smad1 depletion, and qChIP assay indicated an amplification of p53 transactivation in regulating apoptotic genes in the absence of Smad1 (Figure 3J). This evidence concerns the gene SMAD1 and glioblastoma.